Michael Flink

Dr. Flink is a General Clinical Neurologist with interests that include a broad spectrum of neurologic disorders and complaints. In addition, he has special interests in neuromuscular disorders like myasthenia gravis and motor neuron diseases, such as ALS.

He received his Doctor of Osteopathic Medicine (D.O.) in 2004 and Doctor of Philosophy (Ph.D.) in 2003 from Michigan State University as part of the Medical Scientist Training Program. His research involved neuropharmacologic and neurophysiologic approaches to studying neuromuscular disorders. He then went on to complete his Neurology training at the University of California San Diego, where he served as Chief Neurology Resident from 2007-2008. Thereafter, he joined the Department of Neurosciences at the University of California San Diego as an Assistant Clinical Professor from 2008 until 2011, where he had a General Neurology Clinic, and was also the Interim Director of the ALS clinic.

Academic Appointments

2011-Present: Assistant Professor, Michigan State University Department of Neurology, 2012-Present: Director of Neurology Clerkship, Michigan State University Department of Neurology, 2008-2011: Assistant Clinical Professor, Department of Neurosciences, University of California, San Diego, 2009-2011: Interim Director ALS Clinic, Department of Neurosciences, University of California, San Diego

Education

• Ph.D., Pharmacology & Toxicology, Michigan State University; East Lansing, MI 2003
• D.O., Michigan State University College of Osteopathic Medicine; East Lansing, MI 2004
• M.S., Physiology and Biophysics, Georgetown University; Washington, DC 1994
• B.S., Biological Sciences, University of Maryland; College Park, MD 1991

Postdoctoral Training

Neurology Residency, University of California; San Diego, CA 2008, Internship/Preliminary Medicine Residency Training, Michigan State University/Sparrow Health Systems; Lansing, MI 2005

Publications

• Michael Flink and Doris A. Trauner (2009) Toxic and Metabolic Encephalopathies, Clinical Pediatric Neurology, Chapter 9; 117-127; Demos Medical Publishing, New York
• Flink MT, Prado NE and Atchison WD (2008) L-Type Ca2+ channel contribution to release of ACh follows impaired synaptic transmission during passive transfer of Lambert-Eaton syndrome to mice. J Physiol,manuscript in preparation.
• Flink MT and Atchison WD (2003) Ca2+ channels as targets of neurological disease: Lambert-Eaton syndrome and other Ca2+ channelopathies. J. Bioenergetics and Biomembranes 35 (6): 697-718.
• Flink MT and Atchison WD (2003) Iberiotoxin-induced block of Ca2+-activated K+ channels induces dihydropyridine sensitivity of ACh release from mammalian motor nerve terminals. J Pharmacol Exp Ther 305 (2): 646-52.
• Flink MT and Atchison WD (2002) Passive transfer of Lambert-Eaton syndrome to mice induces dihydropyridine sensitivity of neuromuscular transmission. J Physiol 543 (2):567-76.
• Ray P and Flink M (1996) Prevention of botulinum toxin effects via mechanisms involving PLA2 and arachidonic acid. Proc. Medical Defense Bio. Sci. Rev 3:1572-1578.

Clinical Interests

• General Neurology
• Motor neuron diseases (i.e. ALS), neuromuscular disorders, peripheral neuropathies
• Medical Student and Resident Education

Awards

Department of Neurology and Ophthalmology, Michigan State University, Educator of the Year; East Lansing, MI (2011-2012), Johns Hopkins Resident Training Program on Dystonia, Spasticity (2007), Society for Neuroscience Travel Award (2001), Lawrence D. Sills Award for Outstanding Achievement in Research (1996)

Memberships

Michigan Osteopathic Association